U.S. patent number 7,194,307 [Application Number 10/744,952] was granted by the patent office on 2007-03-20 for pacing method and device for preserving native conduction system.
This patent grant is currently assigned to Cardiac Pacemakers, Inc.. Invention is credited to Steven D. Girouard, Bruce H. KenKnight, Joseph M. Pastore, Rodney W. Salo.
United States Patent |
7,194,307 |
Salo , et al. |
March 20, 2007 |
Pacing method and device for preserving native conduction
system
Abstract
An implantable device for delivering cardiac pacing therapy in
order to improve cardiac function is programmed to allow some
amount of intrinsic activity to occur without otherwise the
disturbing the pacing algorithm used to deliver therapy. Intrinsic
cardiac cycles utilize the heart's native conduction system and
thus serve to prevent the atrophy which may otherwise result from
continuous pacing.
Inventors: |
Salo; Rodney W. (Fridley,
MN), KenKnight; Bruce H. (Maple Grove, MN), Pastore;
Joseph M. (Oakdale, MN), Girouard; Steven D. (Woodbury,
MN) |
Assignee: |
Cardiac Pacemakers, Inc. (St.
Paul, MN)
|
Family
ID: |
34679012 |
Appl.
No.: |
10/744,952 |
Filed: |
December 22, 2003 |
Prior Publication Data
|
|
|
|
Document
Identifier |
Publication Date |
|
US 20050137633 A1 |
Jun 23, 2005 |
|
Current U.S.
Class: |
607/27;
607/9 |
Current CPC
Class: |
A61N
1/3684 (20130101); A61N 1/3627 (20130101); A61N
1/36843 (20170801); A61N 1/36842 (20170801) |
Current International
Class: |
A61N
1/368 (20060101) |
Field of
Search: |
;607/9,24,27,28,15 |
References Cited
[Referenced By]
U.S. Patent Documents
Primary Examiner: Evanisko; George R.
Assistant Examiner: Kahelin; Michael
Attorney, Agent or Firm: Schwegman, Lundberg, Woessner &
Kluth, P.A.
Claims
What is claimed is:
1. An implantable cardiac device, comprising: one or more sensing
channels for sensing cardiac electrical activity at one or more
myocardial sites; one or more pacing channels for delivering pacing
pulses to one or more myocardial sites; a controller for
controlling the delivery of pacing pulses in accordance with a
demand pacing mode; and, wherein the controller is programmed to
count the number of paced and intrinsic beats over a defined time
interval and to intermittently reduce the extent of pacing in order
to maintain a desired maximum ratio of paced to intrinsic beats and
to dynamically adjust the desired maximum ratio of paced to
intrinsic beats in accordance with a determination of an amount of
interventricular conduction delay such that the desired maximum
ratio is decreased if the amount of interventricular conduction
delay increases.
2. The device of claim 1 wherein the controller is programmed to
intermittently reduce the extent of pacing by discontinuing pacing
for a specified period of time.
3. The device of claim 1 wherein the controller is programmed to
intermittently reduce the extent of pacing by lengthening an escape
interval.
4. The device of claim 3 wherein the escape interval is an AV delay
interval.
5. The device of claim 1 wherein the controller is programmed to
record an electrogram during an intrinsic beat and dynamically
adjust the desired maximum ratio of paced to intrinsic beats in
accordance with a measured width of a depolarization wave in the
electrogram such that the desired maximum ratio is decreased if the
measured width increases.
6. The device of claim 1 wherein the controller is programmed to
reduce the extent of pacing for a certain amount of time per
specified time period, where the amount of time for which the
extent of pacing is reduced varies with how the count of intrinsic
and paced beats compares with the desired maximum ratio.
7. The device of claim 6 wherein the times when the extent of
pacing is reduced coincide with times at which sleep is expected to
occur.
8. The device of claim 1 further comprising an exertion level
sensor and wherein the extent of pacing is reduced in accordance
with a measured exertion level.
9. The device of claim 1 further comprising: sensing and pacing
channels for the right and left ventricles; and wherein the
controller is programmed to measure the time interval between right
and left ventricular senses during a cardiac cycle and adjust the
desired maximum ratio of paced to intrinsic beats in accordance
therewith.
10. A method for operating an implantable cardiac device,
comprising: sensing cardiac electrical activity at one or more
myocardial sites; delivering pacing pulses in accordance with a
demand pacing mode; counting the number of paced and intrinsic
beats over a defined time interval; intermittently reducing the
extent of pacing in order to maintain a desired maximum ratio of
paced to intrinsic beats; and, dynamically adjusting the desired
maximum ratio of paced to intrinsic beats in accordance with a
determination of an amount of interventricular conduction delay
such that the desired maximum ratio is decreased if the amount of
interventricular conduction delay increases.
11. The method of claim 10 further comprising intermittently
reducing the extent of pacing by discontinuing pacing for a
specified period of time.
12. The method of claim 10 further comprising intermittently
reducing the extent of pacing by lengthening an escape
interval.
13. The method of claim 12 wherein the escape interval is an AV
delay interval.
14. The method of claim 10 further comprising recording an
electrogram during an intrinsic beat and dynamically adjusting the
desired maximum ratio of paced to intrinsic beats in accordance
with a measured width of a depolarization wave in the electrogram
such that the desired maximum ratio is decreased if the measured
width increases.
15. The method of claim 10 further comprising reducing the extent
of pacing for a certain amount of time per specified time period,
where the amount of time for which the extent of pacing is reduced
varies with how the count of intrinsic and paced beats compares
with the desired maximum ratio.
16. The method of claim 15 wherein the times when the extent of
pacing is reduced coincide with times at which sleep is expected to
occur.
17. The method of claim 10 further comprising reducing the extent
of pacing in accordance with a measured exertion level.
18. The method of claim 10 further comprising: sensing the right
and left ventricles; and measuring the time interval between right
and left ventricular senses during a cardiac cycle and adjust the
desired maximum ratio of paced to intrinsic beats in accordance
therewith.
Description
FIELD OF THE INVENTION
This patent application pertains to methods and apparatus for the
treatment of cardiac disease. In particular, it relates to methods
and apparatus for improving cardiac function with
electro-stimulatory therapy.
BACKGROUND
Implantable cardiac devices that provide electrical stimulation to
selected chambers of the heart have been developed in order to
treat a number of cardiac disorders. A pacemaker, for example, is a
device which paces the heart with timed pacing pulses, most
commonly for the treatment of bradycardia where the ventricular
rate is too slow. Atrio-ventricular conduction defects (i.e., AV
block) and sick sinus syndrome represent the most common causes of
bradycardia for which permanent pacing may be indicated. If
functioning properly, the pacemaker makes up for the heart's
inability to pace itself at an appropriate rhythm in order to meet
metabolic demand by enforcing a minimum heart rate. Implantable
devices may also be used to treat cardiac rhythms that are too
fast, with either anti-tachycardia pacing or the delivery of
electrical shocks to terminate atrial or ventricular
fibrillation.
Implantable devices have also been developed that affect the manner
and degree to which the heart chambers contract during a cardiac, a
type of therapy referred to herein as cardiac function therapy
(CFT). The heart pumps more effectively when the chambers contract
in a coordinated manner, a result normally provided by the
specialized conduction pathways in both the atria and the
ventricles that enable the rapid conduction of excitation (i.e.,
depolarization) throughout the myocardium. These pathways conduct
excitatory impulses from the sino-atrial node to the atrial
myocardium, to the atrio-ventricular node, and thence via the
His-Purkinje network to the ventricular myocardium to result in a
coordinated contraction of both atria and both ventricles. This
both synchronizes the contractions of the muscle fibers of each
chamber and synchronizes the contraction of each atrium or
ventricle with the contralateral atrium or ventricle. Without the
synchronization afforded by the normally functioning specialized
conduction pathways, the heart's pumping efficiency is greatly
diminished. Pathology of these conduction pathways and other
inter-ventricular or intra-ventricular conduction deficits can be a
causative factor in heart failure, which refers to a clinical
syndrome in which an abnormality of cardiac function causes cardiac
output to fall below a level adequate to meet the metabolic demand
of peripheral tissues. In order to treat these problems,
implantable cardiac devices have been developed that provide
appropriately timed electrical stimulation to one or more heart
chambers in an attempt to improve the coordination of atrial and/or
ventricular contractions, termed cardiac resynchronization therapy
(CRT). Ventricular resynchronization is useful in treating heart
failure because, although not directly inotropic, resynchronization
can result in a more coordinated contraction of the ventricles with
improved pumping efficiency and increased cardiac output.
Currently, a most common form of CRT applies stimulation pulses to
both ventricles, either simultaneously or separated by a specified
biventricular offset interval, and after a specified
atrio-ventricular delay interval with respect to the detection an
intrinsic atrial contraction.
SUMMARY OF THE INVENTION
The specialized His-Purkinje conduction network of the normal heart
rapidly conducts excitatory impulses from the atrio-ventricular
node to the ventricular myocardium to result in a coordinated
contraction of both ventricles. Artificial pacing with an electrode
fixed into an area of the myocardium does not take advantage of the
heart's native conduction system for conducting excitation
throughout the ventricles, however, because the His-Purkinje
network can only be entered by impulses emanating from the
atrio-ventricular node. Atrophy of the His-Purkinje system may
result from a prolonged period of disuse where there is a lack of
electrical impulses propagating through the system. It has been
shown that some patients with chronic bradycardia who have been
treated with continuous pacing therapy no longer have functional
His-Purkinje conductive tissue distal to the site at which paces
are delivered. In some cases, the cells of the system are replaced
by fibrous tissue (i.e. fibrosis), and is therefore incapable of
propagating electrical impulses.
As noted above, cardiac function therapy may involve pacing the
heart for purposes other than to enforce a particular rhythm. Such
patients may, for example, be chronotropically competent and have
an intact AV conduction pathway. In patients for whom such therapy
is not intended be permanent and who have intact AV conduction
pathways, degeneration of those pathways is an unfortunate
side-effect. The present invention is directed toward a solution of
this problem by providing a device for delivering pacing therapy in
order to improve cardiac function which is programmed to allow some
amount of intrinsic activity to occur without otherwise the
disturbing the pacing algorithm used to deliver therapy. Intrinsic
cardiac cycles utilize the heart's native conduction system and
thus serve to prevent the atrophy which may otherwise result from
continuous pacing. In one embodiment, the device is programmed to
maintain a specified ratio of paced to intrinsic cycles by
temporarily discontinuing pacing for specified or variable time
intervals.
BRIEF DESCRIPTION OF THE DRAWINGS
FIG. 1 is a system diagram of a cardiac device configured for
multi-site stimulation and sensing.
FIG. 2 illustrates an exemplary algorithm for implementing the
invention.
DETAILED DESCRIPTION
As noted above, many patients now receive pacemakers for
non-traditional indications (e.g., cardiac resynchronization
therapy) where ventricular pacing is applied while all or part of
the patient's native conduction system is intact. In these
patients, one would like to pace the ventricle by a method that
preserves the native conduction (His-Purkinje) system. What follows
are descriptions of cardiac function therapy and an exemplary
implantable device for delivering such therapy. Exemplary
algorithms for promoting native conduction during the delivery of
cardiac function therapy are then presented.
1. Cardiac Function Therapy
One example of electro-stimulatory therapy for the purpose of
improving cardiac function is CRT. In ventricular resynchronization
therapy, the ventricles are paced at more than one site in order to
effect a spread of excitation that results in a more coordinated
contraction and thereby overcome interventricular or
intraventricular conduction defects. Biventricular pacing is one
example of resynchronization therapy in which both ventricles are
paced in order to synchronize their respective contractions.
Resynchronization therapy may also involve multi-site pacing
applied to only one chamber. For example, a ventricle may be paced
at multiple sites with excitatory stimulation pulses in order to
produce multiple waves of depolarization that emanate from the
pacing sites. This may produce a more coordinated contraction of
the ventricle and thereby compensate for intraventricular
conduction defects that may exist.
Another type of cardiac function therapy is stress reduction pacing
which involves altering the coordination of ventricular
contractions with multi-site pacing in order to change the
distribution of wall stress experienced by the ventricle during the
cardiac pumping cycle. The degree to which a heart muscle fiber is
stretched before it contracts is termed the preload. The maximum
tension and velocity of shortening of a muscle fiber increases with
increasing preload. The increase in contractile response of the
heart with increasing preload is known as the Frank-Starling
principle. When a myocardial region contracts late relative to
other regions, the contraction of those opposing regions stretches
the later contracting region and increases the preload. The degree
of tension or stress on a heart muscle fiber as it contracts is
termed the afterload. Because pressure within the ventricles rises
rapidly from a diastolic to a systolic value as blood is pumped out
into the aorta and pulmonary arteries, the part of the ventricle
that first contracts due to an excitatory stimulation pulse does so
against a lower afterload than does a part of the ventricle
contracting later. Thus a myocardial region that contracts later
than other regions is subjected to both an increased preload and
afterload. This situation is created frequently by the ventricular
conduction delays associated with heart failure and ventricular
dysfunction. The heart's initial physiological response to the
uneven stress resulting from an increased preload and afterload is
compensatory hypertrophy in those later contracting regions of the
myocardium. In the later stages of remodeling, the regions may
undergo atrophic changes with wall thinning due to the increased
stress. The parts of the myocardium that contract earlier in the
cycle, on the other hand, are subjected to less stress and are less
likely to undergo hypertrophic remodeling.
The degree of wall stress experienced by a myocardial site during
systole is thus dependent upon the time at which that site
contracts relative to other myocardial sites. Reversal of
remodeling may be effected by pacing one or more sites in a
ventricle (or an atrium) with one or more excitatory stimulation
pulses during a cardiac cycle with a specified pulse output
sequence. The spread of excitation from a ventricular pacing site
is not conducted by the His-Purkinje system but must proceed only
via the much slower conducting ventricular muscle fibers, resulting
in the part of the ventricular myocardium stimulated by the pacing
electrode contracting well before parts of the ventricle located
more distally to the electrode. Pacing therapy can therefore be
delivered in a manner that excites one or more previously stressed
and remodeled regions of the myocardium earlier during systole so
that they experience less afterload and preload. Pre-excitation of
a remodeled region relative to other regions unloads the region
from mechanical stress and allows reversal of remodeling to
occur.
2. Exemplary Implantable Device
An implantable cardiac device is typically placed subcutaneously or
submuscularly in a patient's chest with leads threaded
intravenously into the heart to connect the device to electrodes
used for sensing and stimulation. Leads may also be positioned on
the epicardium by various means. A programmable electronic
controller causes the stimulus pulses to be output in response to
lapsed time intervals and sensed electrical activity (i.e.,
intrinsic heart beats not as a result of a stimulus pulse). The
device senses intrinsic cardiac electrical activity by means of
internal electrodes disposed near the chamber to be sensed. A
depolarization wave associated with an intrinsic contraction of the
atria or ventricles that is detected by the device is referred to
as an atrial sense or ventricular sense, respectively. In order to
cause such a contraction in the absence of an intrinsic beat, a
stimulus pulse (a.k.a. a pace or pacing pulse when delivered in
order to enforce a certain rhythm) with energy above a certain
threshold is delivered to the chamber.
FIG. 1 shows a system diagram of a microprocessor-based cardiac
device suitable for practicing the present invention. The device is
equipped with multiple sensing and pacing channels which may be
physically configured to sense and/or pace multiple sites in the
atria or the ventricles. The device shown in FIG. 1 can be
configured for cardiac resynchronization pacing of the atria or
ventricles and/or for myocardial stress reduction pacing such that
one or more cardiac sites are sensed and/or paced in a manner that
pre-excites at least one region of the myocardium. The multiple
sensing/stimulation channels may be configured, for example, with
one atrial and two ventricular sensing/stimulation channels for
delivering biventricular resynchronization therapy, with the atrial
sensing/stimulation channel used to deliver biventricular
resynchronization therapy in an atrial tracking mode as well as to
pace the atria if required. The controller 10 of the pacemaker is a
microprocessor which communicates with a memory 12 via a
bidirectional data bus. The memory 12 typically comprises a ROM
(read-only memory) for program storage and a RAM (random-access
memory) for data storage. The controller could be implemented by
other types of logic circuitry (e.g., discrete components or
programmable logic arrays) using a state machine type of design,
but a microprocessor-based system is preferable. As used herein,
the term "circuitry" should be taken to refer to either discrete
logic circuitry or to the programming of a microprocessor.
Shown in the figure are four exemplary sensing and pacing channels
designated "a" through "d" comprising bipolar leads with ring
electrodes 34a d and tip electrodes 33a d, sensing amplifiers 31a
d, pulse generators 32a d, and channel interfaces 30a d. Each
channel thus includes a pacing channel made up of the pulse
generator connected to the electrode and a sensing channel made up
of the sense amplifier connected to the electrode. The channel
interfaces 30a d communicate bidirectionally with microprocessor
10, and each interface may include analog-to-digital converters for
digitizing sensing signal inputs from the sensing amplifiers and
registers that can be written to by the microprocessor in order to
output pacing pulses, change the pacing pulse amplitude, and adjust
the gain and threshold values for the sensing amplifiers. The
electrodes of each bipolar lead are connected via conductors within
the lead to a MOS switching network 70 controlled by the
microprocessor. The switching network is used to configure a
sensing channel by switching electrodes to the input of a sense
amplifier in order to detect intrinsic cardiac activity and
configure a pacing channel by switching electrodes to the output of
a pulse generator in order to deliver a pacing pulse. The switching
network also enables the device to sense or pace either in a
bipolar mode using both the ring and tip electrodes of a lead or in
a unipolar mode using only one of the electrodes of the lead with
the device housing or can 60 serving as a ground electrode. As
explained below, one way in which the device may alter the spatial
distribution of pacing is to switch from unipolar to bipolar pacing
(or vice-versa) or to interchange which electrodes of a bipolar
lead are the cathode and anode during bipolar pacing. A shock pulse
generator 50 is also interfaced to the controller for delivering a
defibrillation shock via a pair of shock electrodes 51 to the atria
or ventricles upon detection of a shockable tachyarrhythmia.
The controller 10 controls the overall operation of the device in
accordance with programmed instructions stored in memory, including
controlling the delivery of paces via the pacing channels,
interpreting sense signals received from the sensing channels, and
implementing timers for defining escape intervals and sensory
refractory periods. The sensing circuitry of the pacemaker detects
a chamber sense, either an atrial sense or ventricular sense, when
an electrogram signal (i.e., a voltage sensed by an electrode
representing cardiac electrical activity) generated by a particular
channel exceeds a specified detection threshold. Pacing algorithms
used in particular pacing modes employ such senses to trigger or
inhibit pacing, and the intrinsic atrial and/or ventricular rates
can be detected by measuring the time intervals between atrial and
ventricular senses, respectively. A sensing channel may also be
configured to record an electrogram for morphology analysis, where
the electrogram may be an intra-cardiac electrogram generated by a
sensing/pacing electrode within the heart or a so-called
subcutaneous ECG generated by a subcutaneously disposed electrode.
A telemetry interface 40 is also provided which enables the
controller to communicate with an external programmer.
An exertion level sensor 330 (e.g., an accelerometer, a minute
ventilation sensor, or other sensor that measures a parameter
related to metabolic demand) enables the controller to adapt the
pacing rate in accordance with changes in the patient's physical
activity. In one embodiment, the exertion level sensor is a minute
ventilation sensor which includes an exciter and an impedance
measuring circuit. The exciter supplies excitation current of a
specified amplitude (e.g., as a pulse waveform with constant
amplitude) to excitation electrodes that are disposed in the
thorax. Voltage sense electrodes are disposed in a selected region
of the thorax so that the potential difference between the
electrodes while excitation current is supplied is representative
of the transthoracic impedance between the voltage sense
electrodes. The conductive housing or can may be used as one of the
voltage sense electrodes. The impedance measuring circuitry
processes the voltage sense signal from the voltage sense
electrodes to derive the impedance signal. Further processing of
the impedance signal allows the derivation of signal representing
respiratory activity and/or cardiac blood volume, depending upon
the location the voltage sense electrodes in the thorax. (See,
e.g., U.S. Pat. Nos. 5,190,035 and 6,161,042, assigned to the
assignee of the present invention and hereby incorporated by
reference.) If the impedance signal is filtered to remove the
respiratory component, the result is a signal that is
representative of blood volume in the heart at any point in time,
thus allowing the computation of stroke volume and, when combined
with heart rate, computation of cardiac output.
The controller is capable of operating the device in a number of
programmed pacing modes which define how pulses are output in
response to sensed events and expiration of time intervals. Most
pacemakers for treating bradycardia are programmed to operate
synchronously in a so-called demand mode where sensed cardiac
events occurring within a defined interval either trigger or
inhibit a pacing pulse. Inhibited demand pacing modes utilize
escape intervals to control pacing in accordance with sensed
intrinsic activity such that a pacing pulse is delivered to a heart
chamber during a cardiac cycle only after expiration of a defined
escape interval during which no intrinsic beat by the chamber is
detected. Escape intervals for ventricular pacing can be restarted
by ventricular or atrial events, the latter allowing the pacing to
track intrinsic atrial beats. An AV delay interval, for example, is
a ventricular escape interval started by an atrial sense in an
atrial tracking mode and started by an atrial pace in an AV
sequential pacing mode Cardiac function therapy, whether for the
purpose of cardiac resynchronization or for reversal of remodeling,
is most conveniently delivered in conjunction with a bradycardia
pacing mode where, for example, multiple excitatory stimulation
pulses are delivered to multiple sites during a cardiac cycle in
order to both pace the heart in accordance with a bradycardia mode
and provide pre-excitation of selected sites.
A particular pacing mode for delivering cardiac function therapy,
whether for stress reduction or resynchronization, includes a
defined pulse output configuration and pulse output sequence, where
the pulse output configuration specifies a specific subset of the
available electrodes to be used for delivering pacing pulses and
the pulse output sequence specifies the timing relations between
the pulses. The pulse output configuration is defined by the
controller selecting particular pacing channels for use in
outputting pacing pulses and by selecting particular electrodes for
use by the channel with switch matrix 70. The pulse output
configuration and sequence which optimally effects reverse
remodeling by selectively reducing myocardial wall stress may or
may not be the optimum pulse output configuration and sequence for
maximizing hemodynamic performance by resynchronizing ventricular
contractions. For example, a more hemodynamically effective
contraction may be obtained by exciting all areas of the myocardium
simultaneously, which may not effectively promote reversal of the
hypertrophy or remodeling.
3. Pacing Algorithms for Preserving Native Conduction System
The present invention involves the promotion of impulses from the
native His-Purkinje system in a pacemaker patient by programming an
implantable device to reduce the extent of ventricular pacing at
fixed or variable intervals so that His-Purkinje cells continue to
be stimulated and do not undergo atrophy or fibrosis. Reduction of
the extent of ventricular pacing may involve the temporary complete
withdrawal of pacing therapy or, in the case of a chronotropically
incompetent patient, temporary reversion to an atrial-only pacing
mode. In another variation, reduction of the extent of pacing may
be effected by the device prolonging the paced AV interval in an
atrial tracking or AV sequential pacing mode or other ventricular
escape interval so that more intrinsic ventricular beats occur
after atrial events or so that more partially intrinsic or fusion
beats (i.e., beats made up of both intrinsic and paced excitation)
occur which partially activate the native His-Purkinje system.
These different means for reducing the extent of pacing may be
implemented in different ways as in the embodiments described
below.
In a one embodiment, a cardiac function device is programmed to
allow a certain maximum ratio of paced beats to intrinsic conducted
beats. The ratio may also be programmably specified by a clinician.
FIG. 2 illustrates an exemplary algorithm for maintaining a
specified maximum ratio R of paced to intrinsic beats. At step 201,
the device clears counters M and N which are used to maintain
counts of paced and intrinsic beats, respectively. At step 202, the
device waits for the next beat to occur. At step 203, either M or N
is incremented depending on whether the beat is paced or intrinsic,
respectively. At step 204, the total number of counted beats is
compared with a specified number T which represents how many beats
must be counted before the ratio is computed and compared with R.
In an alternate embodiment, beats may be counted for a specified
period of time before the ratio is computed and tested. At step
205, the ratio M/N of paced to intrinsic beats over the previous
total T beats (or, alternatively, over a specified time period) is
computed and compared with the desired ratio R. If the computed M/N
ratio is less than or equal to R, the device returns to step 201.
If the computed ratio is greater than the desired maximum value R,
the extent of pacing is reduced at step 206. After the period
during which the extent of pacing is reduced ends, the device
returns to step 201.
In another embodiment, the device is programmed to enable intrinsic
beats by reducing the extent of pacing for a certain amount of time
per day (e.g. 1 hour per day) or other time period. (e.g., 12 hours
per week). The amount of time for which the extent of pacing is
reduced may be made to increase if the computed M/N ratio is
greater than R. The times when the extent of pacing is reduced may
be selected to coincide with the times at which specific events
such as sleep or exercise are expected to occur. Alternatively, the
device may use an exertion level sensor to detect periods of
activity or non-activity and then reduce the extent of pacing
accordingly. Whether it is desirable to reduce the extent of pacing
as part of cardiac function therapy while the patient is active or
while the patient is at rest will largely depend on the purpose of
the cardiac function therapy. In cases where the cardiac function
therapy is intended to increase cardiac output (i.e., CRT), it may
be desirable to reduce the extent of therapy only when the patient
is non-active. If the therapy is intended to redistribute wall
stress for reversal of cardiac remodeling, on the other hand, such
therapy may not be hemodynamically enhancing so that reduction of
the extent of such therapy may most advantageously take place when
the patient is active. The device may also have the capability of
measuring cardiac output so that temporary reductions in the extent
of pacing may take place as determined by the level of cardiac
output rather than activity level.
In another embodiment, the state of the patient's conduction system
is assessed by determining the patient's interventricular
conduction delay. An increased interventricular conduction delay
indicates a worsening of the patient's conduction system. An
implantable device may determine the interventricular conduction
delay by measuring the interval between right and left ventricular
senses during a cardiac cycle or by measuring the width of a
ventricular depolarization waveform (i.e., an R wave or QRS wave)
in an electrogram. If the patient's conduction system is found to
be worsening, the extent of reduction in pacing can be increased
and vice-versa. For example, the maximum ratio R paced to intrinsic
beats may be dynamically determined by the implantable device
assessing the conduction velocity during one or more intrinsic
beats from a recorded intra-cardiac or subcutaneous electrogram or
by measuring the time interval between senses of differently placed
ventricular sensing electrodes. If the conduction velocity shows
progressive slowing, it may be assumed that deterioration of the
native conduction system is occurring. The device may then increase
the proportion of intrinsic beats to counteract this process. For
example, the device may be programmed to record an electrogram
during an intrinsic beat and dynamically adjust the desired maximum
ratio of paced to intrinsic beats in accordance with a measured
width of a depolarization wave in the electrogram such that the
desired maximum ratio is decreased if the measured width
increases.
In another embodiment, rather than temporarily reducing the extent
of pacing, the device may be configured to deliver pacing therapy
in a manner which promotes intrinsic activity. For example, in the
case where the patient has an implanted device configured for
biventricular pacing, the device may be programmed to periodically
switch between right ventricular pacing and left ventricular pacing
with a long enough AV delay to guarantee intrinsic activation of
the non-paced ventricle. This would be done often enough to
guarantee that both conduction systems (right and left side) remain
healthy.
Although the invention has been described in conjunction with the
foregoing specific embodiments, many alternatives, variations, and
modifications will be apparent to those of ordinary skill in the
art. Such alternatives, variations, and modifications are intended
to fall within the scope of the following appended claims.
* * * * *